Specific tolerance to the hapten, p-azobenzenearsonate, can be induced in neonatal and adult mice when the hapten is presented in the form of a conjugate to the protein human gamma globulin. The adult tolerant state is characterized by a 5-10 fold decrease in total anti-ABA titer and preferential loss of the clones of B-cells capable of producing antibody of the major idiotype. The mechanism of this has been shown to be due to a mixture of T-cell suppression (presumably idiotype specific), B-cell dominance, and clonal elimination of both idiotype positive and idiotype negative B-cell precursors. Other studies have shown that the T-cell and B-cell responses of certain strains of mice to BSA is under control of genes mapping within the MHC. Mapping studies indicate that both gene complementation and single locus control can be exerted. The same pattern of high and low responsiveness is observed when individual domains of BSA are used as immunogens.